Given the important role of debridement in facilitating successful wound healing, these authors discuss pertinent issues concerning the timing and degree of debridement, and offer their perspectives on debridement modalities ranging from enzymatic agents to ultrasonic debridement and hydrosurgery.
Debridement is often a key element in effective wound care. Recently, the wound healing community endeavored to create guidelines in an effort to help standardize debridement.1 There will always be a certain amount of artistry in sharp surgical debridement (as there is with surgery), but the question is, “Are we debriding too much?”
The frequency and aggressiveness with which we debride varies greatly from practitioner to practitioner. Training of the clinician, available resources and fee for service can factor into how frequently we debride an ulcer. The fee-for-service model can potentially increase the frequency and extent of debridement. As healthcare moves from a fee for service model to a value-based paradigm, providing the most high quality, cost-effective treatment is all that matters. We must learn to heal wounds quicker and with lower cost. Improving our techniques and protocols for effective debridement will help us meet this challenge. Value-based medicine demands superior outcomes.
As wound care has evolved, the treatments have improved through trial and error. Through careful observation, we better understand the underlying science of wound healing. Wound debridement has long been established to be necessary for enhancing wound healing. More recently, we have developed a better understanding of the reasons why.
Before wound care specialists ever get out a curette or tissue nipper, there is critical information they need to obtain. One should determine the etiology of the wound. Debriding a pyoderma gangrenosum actually causes the ulcer to worsen due to stimulation of the inflammatory cascade. What are the comorbidities of the patient? One must evaluate the vascular status. Determining local perfusion is particularly important when debriding wounds on the distal aspect of the foot.2 Although offloading is not the focus of this discussion, it is imperative to offload plantar ulcers properly. Neither the most meticulous debridement nor the latest technology can overcome inadequate offloading.
Additionally, the chronicity of the wound and amount of bioburden are factors that reduce normal wound healing. Chronic ulcers may have developed secondary to a myriad of etiologies including trauma, surgery, pressure, metabolic, venous and arterial etiologies, and diabetic neuropathy. Bioburden is like a wall that allows bacteria to be protected from the host’s defenses. Biofilms are often recalcitrant to routine surgical debridement.3
The three most prevalent agents to reduce bioburden are iodine, silver and honey. Iodosorb (Smith and Nephew) is able to reduce bioburden, control exudate and provide a measure of debridement. The use of silver and honey products is well documented. Maggot therapy is another modality that can help reduce bioburden while also debriding the wound.
So why is debridement so important? Debridement has the following purposes.4,5
• Debridement reduces bioburden to help control or reduce infection. Even if an ulcer is not “infected,” the bacterial bioburden causes increased local inflammation.
• Debridement allows more accurate visualization of the wound base and edges, which allows for more precise staging.
• Debridement removes necrotic/non-viable tissue, which impedes wound healing, causes protein loss and can be a nidus for infection.
• Debridement stimulates new circulation (angiogenesis) and allows adequate oxygen delivery to the wound.
• Debridement removes undermining and tunneling, and may help reduce abscess formation.
• Debridement releases healing growth factors at the edge of the wound.
• Debridement prepares the wound bed by leaving only tissues that are capable of regenerating.
Studies by Steed, Williams and their respective colleagues found that sharp debridement of wounds resulted in increased healing rates in comparison to wounds that were not debrided.6,7 These well-known studies validated our debriding of wounds but again, are we debriding too much?
There are no concrete guidelines on wound debridement. In May of this year, the European Wound Management Association put out a nearly 50-page document on debridement.1 They recommend a debridement algorithm based on the consensus opinion of the authors. The reality is that there is a lack of standardized guidelines for wound debridement.
On a microscopic level, the cells at the wound edge are not functioning properly and the wound pathway has been disturbed. Keratinocytes at and beyond the callused wound edge have become disoriented and have lost their ability to communicate. Researchers have shown that these chronic wound keratinocytes do not have receptors for growth factors.8
The thought is that biomarkers can identify these dysfunctional keratinocytes. Early evidence has identified three of these biomarkers that may act as a “molecular scalpel.”8 This scalpel would give us a cellular/molecular basis for debridement. As exciting as this is, the practicality of its use will depend on the cost-to-benefit ratio and only time will tell. Regardless of whether we ever get to use a molecular scalpel, re-establishing the normal physiological function of the cells at the wound edge is essential for healing of the ulcer.
So how do we accomplish this objective? Sharp debridement and other direct debridement techniques are effective but again, there are questions on frequency and to what extent.
At what point do we stop debriding? Do you start with aggressive sharp debridement? This initial procedure along with appropriate copious lavage provides a “complete” debridement that helps to manage infection, bioburden and a chronic wound. Clinicians would subsequently follow this with maintenance debridement and aggressive wound cleansing (e.g. slough removal with gauze). These subsequent debridements require greater thought and consideration of options. Debridement that is too aggressive, especially at the wound edge, can damage the framework for healing.
A consensus guidance from the United Kingdom in 2010 attempted to address this lack of standardization.9 In terms of debridement, the authors recommended that prior to debridement, the clinician should consider the following:
What is the goal of debridement?
How quickly does one need to achieve this goal?
What is the best modality for accomplishing the debridement?
Not all wounds need debridement and we as wound care specialists need to avoid tunnel vision. A well-adhered eschar that is not infected will be better served if we leave it alone. If the wound has minimal devitalized tissue, even the most skilled doctors cannot be 100 percent sure of the precision of their debridement.
When the tissue within the wound bed is devitalized, how do we get the benefits of debridement without inhibiting wound healing by being too aggressive? This is where newer technologies shine. Products like DermaPACE (Sanuwave) and low energy ultrasound may obviate the need for mechanical or surgical debridement by stimulating an inflammatory response and causing the release of growth factors that lead to angiogenesis and cell proliferation.
Iatrogenic trauma of “healthy” tissue due to overly aggressive wound debridement can delay the healing process.
A poorly planned bone biopsy can create unnecessary trauma, which can often lead to more extensive bone infection and wound complications. Should we debride exposed bone? The old adage is that exposed bone is infected until proven otherwise. However, if the bone has normal color and consistency, is it more appropriate to use Vacuum Assisted Closure (VAC Therapy, KCI) and some sort of graft? Violating the cartilage or bony cortex may result in iatrogenic trauma to the natural barrier that had been present. This in turn would lead to seeding bacteria with the end result being osteomyelitis. One will most likely encounter these concerns with heel and midfoot ulcers, for example. For similar digital ulcers, are we better off performing bony debridement (to clear the wound margins) and subsequent primary closure to achieve optimal closure rates?
Here is a succinct review of the types of debridement.
Surgical (sharp) debridement. Surgical debridement is the quickest and most efficient method of debridement. It is the preferred method if there is concern of infection or abscess. This technique is quick and selective, but very user dependent.
Mechanical debridement. In mechanical debridement, a saline-moistened dressing dries overnight and adheres to the dead tissue. Removing the dressing pulls away the dead tissue. This process is one of the oldest methods of debridement. It can be very painful because the dressing can adhere to living as well as non-living tissue. It is non-selective and considered an unacceptable debridement method for clean wounds. Whirlpool therapy, gauze, paraffin and monofilament fiber pads are other examples of mechanical debridement.
Enzymatic debridement. This technique makes use of certain enzymes and other compounds to dissolve necrotic tissue. It is highly selective. Proteolytic enzymes hydrolyze peptide bonds, which helps to facilitate removal of non-viable tissue from the wound. These enzymes work synergistically with the wound’s endogenous enzymes. One then places a moist dressing over the wound. Enzymatic debridement is faster than autolytic debridement but more conservative than sharp surgical debridement.
Santyl (Healthpoint Biotherapeutics) is the most common product in this category. Santyl is a once-daily prescription product with no generic equivalent (other enzymes that have been derived from other sources have not gone through the FDA process). This collagenase ointment works from the bottom up by selectively degrading (dissolving) collagen anchored to the wound. It only breaks down denatured collagen, leaving other proteins unaffected. Also, it doesn’t harm the collagen needed to form a scaffold, which is crucial for healing during the second phase of the wound healing cascade.
Autolytic debridement. This process takes advantage of the body’s own endogenous enzymes to remove necrotic tissue slowly. The key to the technique is keeping the wound moist as these dressings are occlusive, which helps to saturate the wound. These dressings help trap wound fluid that contains the growth factors, enzymes and immune cells that promote wound healing. Autolytic debridement is more selective than any other debridement method but it also takes the longest time to work. It is inappropriate for wounds that have become infected. Patients usually change these dressings every two to three days. It is necessary to take precautions to protect the periwound from maceration.
Examples include: hydrocolloids, hydrogels, highly absorptive dressings (Sorbion Sachet S, Carolon Health Care Products), hydrofibers (Aquacel, ConvaTec) and iodine-based preparations such as Iodosorb (Smith & Nephew). Sorbion Sachet S is a cellulose fiber pad with gelling agents. It allows gentle debridement of the wound, provides anti-inflammatory action and removes excessive exudate.
Larval therapy. Maggot therapy (biosurgery) is a form of biological debridement known since antiquity. The larvae of Lucilia sericata (green bottle fly) secrete enzymes that break down necrotic tissue into a liquid. The larvae then ingest this liquid. The maggot secretions also contain antibacterial substances. They also promote wound healing and amplify human fibroblast and chondrocyte growth. The method is rapid and selective although patients are usually reluctant to submit to the procedure.
Typically, one would place larvae in the wound bed twice a week and leave them in place for 24 to 72 hours with a recommended dose of 10 to 15 larvae per cm2. One can also utilize maggot therapy with a biobag, which contains the larvae and prevents escape.
Ultrasound debridement. Depending on frequency and intensity, ultrasound can exert a range of effects on ulcers. This versatility allows one to use ultrasound on nearly every type of wound. The benefits of ultrasound are evident in the cavitation effect and the direct stimulation of cells.
In cavitation, bursting microbubbles assist in the fibrinolytic separation of denatured protein, which results in selective debridement and fragmentation of non-viable tissue. Cavitation also can have a direct bactericidal effect.
The stimulation of cells (via fluid shear stress) causes the release of nitrous oxide. This subsequently results in resolution of the vasospasm, thereby increasing blood flow around the wound. Additionally, fibroblasts, macrophages and endothelial cells are stimulated.10
Examples of ultrasound debridement products include Qoustic Wound Therapy System (Arobella Medical) and SonicOne (Misonix). The Qoustic Wound Therapy System delivers focused ultrasonic energy as it lightly contacts the wound bed, gently separating and removing unwanted tissue while preserving healthy granulation tissue.
Hydrosurgery. Jet lavage debridement is the evolution of wound irrigation. Clinicians can use the irrigation from hydrosurgery to physically remove debris, loose tissue, etc., from the wound. There are a number of hydrosurgery products. Some are gentle while others are almost like a surgical water knife. The versatility of hydrosurgery intensities enables clinicians to use these devices on almost all types of wounds.
Examples of these devices include MIST Therapy (Celleration) and the Versajet (Smith and Nephew). MIST Therapy is a painless, low frequency, low intensity, non-thermal, non-contact ultrasound-generated mist. Promoting healing by mechanical cell stimulation, MIST Therapy allows clinicians to perform gentle wound debridement that reportedly reduces the wound’s bacterial bioburden and increases angiogenesis.11
Another potential benefit is the possible use of antibiotic/antiseptic solutions (super-oxidized solutions and polyhexanide solutions) instead of saline. When one uses a hydrosurgical device in conjunction with antiseptic irrigation, it may act as a physical and biological debrider.
Super-oxidized solution is a hypotonic solution that contains hypochlorous acid, sodium hypochlorite, chlorine dioxide, ozone, hydrogen peroxide and sodium chloride. Super-oxidized solution is an electrochemically processed aqueous solution manufactured from pure water and sodium chloride. Reactive species of oxygen and chlorine (which have formed via electrolysis) create an unbalanced osmolarity. This disparity in osmolarity subsequently causes damage to the integrity of the cell membrane and then reacts and denatures the lipids and proteins of single cell organisms. This is a direct result of the osmolarity difference between the ion concentrations of the solution and single cell organism.
Multicellular organisms are not prone to such osmolarity changes, which is why these solutions are safe to use on the wound. An example of a super-oxidized solution would be Microcyn (Oculus Innovative Services).
Polyhexanide is a positively charged polymer that works against negatively charged microorganisms. It is able to penetrate slough and bioburden to stimulate wound healing. Polyhexanide is able to lower wound surface tension, which then supports the physical removal of debris and bacteria from the wound bed. It also has excellent antimicrobial properties, which makes the modality useful for surgical prep. One product example would be B Braun Medical’s Prontosan Wound Irrigation Solution and Wound Gel with Polyhexanide.
As wound care continues to evolve, the wound care specialist will be looking for ways to avoid excessive debridement. Regardless of the reason, iatrogenic trauma to the wound due to overly aggressive debridement cannot continue. We have to take responsibility. We cannot let fee for service, lack of training or being in a rush cause actions that result in the delay of wound healing. In the future, there may be tests that can determine if the ulcer has had adequate debridement.
Products like DermaPACE and the Qoustic device give us new tools to stimulate wound healing without the trauma of sharp debridement. One should consider alternative methods to sharp surgical debridement when the wound bed is covered in fibrin or slough, or if the wound is of partial thickness and the wound edges are not clearly demarcated.
Debridement is only a portion of the equation for a wound to heal and a multidisciplinary team approach is essential for wound healing. Without proper nutrition, effective management of comorbidities, control of any infection and providing for adequate vascularity, the wound cannot function properly. Until we restore this delicate balance, the wound will not heal. The aggressive implementation of offloading devices, the timely application of the “best” wound dressings that can absorb exudate and the appropriate use of biologics to stimulate wound healing are key elements to restore this balance and facilitate an environment for wound healing.
Dr. Belken is in private practice at Foot Healthcare Associates in Michigan. He is an Associate of the American College of Foot and Ankle Surgeons.
Dr. Mozen is in private practice at Foot Healthcare Associates in Michigan. He is a Diplomate of the American Board of Podiatric Surgery and a Fellow of the American College of Foot and Ankle Surgeons.
1. European Wound Management Association Document: Debridement. Available at http://ewma.org/english/ewma-news/show/article/ewma-document-on-debridem... . Published Jan. 8, 2013. Accessed July 9, 2013.
2. Armstrong DG, Mulder G, Seaman S. Standard, appropriate, and advanced care and medical-legal considerations: part one - diabetic foot ulcerations. Wounds. 2003; 15(4):92-106.
3. Percival SL, Bowler P, Woods EJ. Assessing the effect of antimicrobial wound dressings on biofilms. Wound Repair Regen. 2008; 16(1):52-57.
4. Falanga V, Harding KG (eds.). The Clinical Relevance of Wound Bed Preparation. Springer Verlag, New York, 2002.
5. Ayello E, Cuddigan J, Kerstein MD. Skip the knife: debriding wounds without surgery. Nursing. 2002; 32(9):58-63.
6. Steed DL, Donohoe D, Webster MW, Lindsley L. Effect of extensive debridement and treatment on healing of diabetic foot ulcers. Diabetic Ulcer Study Group. J Am Coll Surg. 1996; 183(1):61-4.
7. Williams D, Enoch S, Miller D, et al. Effect of sharp debridement using curette on recalcitrant nonhealing venous leg ulcers: a concurrently controlled, prospective cohort study. Wound Repair Regen. 2005; 13(2):131-7.
8. Tanic-Canic M. Should we debride wounds? Portal Education. Online lecture from the Diabetic Foot Global Conference, 2013.
9. Gray D, Acton C, Chadwick P, et al. Consensus guidance for the use of debridement techniques in the UK. Wounds UK. 2011; 7(1):77-84.
10. Kavos SJ, Liedl DL, Boon AJ, et al. Expedited wound healing with noncontact, low-frequency ultrasound therapy in chronic wounds: a retrospective analysis. Adv Skin Wound Care. 2008; 21(9):416-423.
11. Available at http://www.celleration.com/mist-therapy/  .
12. Andros G, Armstrong DG, et al. Consensus statement on negative pressure wound therapy (V.A.C.® Therapy) for the management of diabetic foot wounds. Ostomy Wound Manage. 2006; 52(Suppl):1-32.
13. Wang CJ, Kuo YR, Wu RW, et al. Extracorporeal shockwave treatment for chronic diabetic foot ulcers. J Surg Res. 2009; 152(1):96-103.
For further reading, see “Pertinent Insights On Effective Debridement Tools” in the September 2011 issue of Podiatry Today or “Current Concepts In Wound Debridement” in the July 2009 issue.